The human leukemic oncogene MLL-AF4 promotes hyperplastic growth of hematopoietic tissues in Drosophila larvae
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M. Therrien | Helene Knævelsrud | Jorrit M. Enserink | M. Formica | Amani Al Outa | Miriam Aarsund | J. A. Johannessen | Nora Rojahn Bråthen | Aina Louise C. Haukeland
[1] E. Clappier,et al. The KMT2A recombinome of acute leukemias in 2023 , 2023, Leukemia.
[2] S. Armstrong,et al. The menin inhibitor revumenib in KMT2A-rearranged or NPM1-mutant leukaemia , 2023, Nature.
[3] V. Honti,et al. Peeling Back the Layers of Lymph Gland Structure and Regulation , 2022, International journal of molecular sciences.
[4] Elias A. Rahal,et al. Expression of chronic myeloid leukemia oncogenes BCR-ABL P210 and BCR-ABL T315I affect cellular and humoral innate immunity in Drosophila melanogaster , 2022, microPublication biology.
[5] A. Mead,et al. A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program , 2021, Nature Communications.
[6] M. Konopleva,et al. Outcomes of acute lymphoblastic leukemia with KMT2A (MLL) rearrangement: the MD Anderson experience , 2021, Blood advances.
[7] R. Marschalek,et al. The role of reciprocal fusions in MLL-r acute leukemia: studying the chromosomal translocation t(4;11) , 2021, Oncogene.
[8] M. Konopleva,et al. Predictors of outcomes in adults with acute myeloid leukemia and KMT2A rearrangements , 2021, Blood Cancer Journal.
[9] N. Perrimon,et al. Preparation of Drosophila Larval Blood Cells for Single-cell RNA Sequencing. , 2021, Bio-protocol.
[10] R. Marschalek,et al. The role of reciprocal fusions in MLL-r acute leukemia: studying the chromosomal translocation t(6;11) , 2021, Oncogene.
[11] G. Sauvageau,et al. A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene , 2021, PLoS genetics.
[12] Y. Yao,et al. Small-molecule inhibitor of AF9/ENL-DOT1L/AF4/AFF4 interactions suppresses malignant gene expression and tumor growth , 2021, Theranostics.
[13] Editor's evaluation: Paths and pathways that generate cell-type heterogeneity and developmental progression in hematopoiesis , 2021 .
[14] W. Foulkes,et al. Achieving clinical success with BET inhibitors as anti-cancer agents , 2021, British Journal of Cancer.
[15] V. Honti,et al. There and back again: The mechanisms of differentiation and transdifferentiation in Drosophila blood cells. , 2020, Developmental biology.
[16] R. Nasr,et al. The Leukemic Fly: Promises and Challenges , 2020, Cells.
[17] L. Jin,et al. The Posterior Signaling Center Is an Important Microenvironment for Homeostasis of the Drosophila Lymph Gland , 2020, Frontiers in Cell and Developmental Biology.
[18] R. Marschalek. The reciprocal world of MLL fusions: A personal view. , 2020, Biochimica et biophysica acta. Gene regulatory mechanisms.
[19] R. Slany. MLL fusion proteins and transcriptional control. , 2020, Biochimica et biophysica acta. Gene regulatory mechanisms.
[20] N. Perrimon,et al. Single-cell transcriptome maps of myeloid blood cell lineages in Drosophila , 2020, Nature Communications.
[21] K. Ross,et al. A Menin-MLL Inhibitor Induces Specific Chromatin Changes and Eradicates Disease in Models of MLL-Rearranged Leukemia. , 2019, Cancer cell.
[22] R. Nasr,et al. Validation of a Drosophila model of wild-type and T315I mutated BCR-ABL1 in chronic myeloid leukemia: an effective platform for treatment screening , 2019, Haematologica.
[23] U. Banerjee,et al. Drosophila as a Genetic Model for Hematopoiesis , 2019, Genetics.
[24] S. Armstrong,et al. The DOT1L inhibitor pinometostat reduces H3K79 methylation and has modest clinical activity in adult acute leukemia. , 2018, Blood.
[25] H. Bourbon,et al. Genome Regulation by Polycomb and Trithorax: 70 Years and Counting , 2017, Cell.
[26] T. Cheng,et al. PBX3 is essential for leukemia stem cell maintenance in MLL‐rearranged leukemia , 2017, International journal of cancer.
[27] H. Munshi,et al. BET inhibitors in the treatment of hematologic malignancies: current insights and future prospects , 2016, OncoTargets and therapy.
[28] R. Majeti,et al. ASH1L Links Histone H3 Lysine 36 Dimethylation to MLL Leukemia. , 2016, Cancer discovery.
[29] R. Slany. The molecular mechanics of mixed lineage leukemia , 2016, Oncogene.
[30] S. Malek,et al. Menin-MLL inhibitors block oncogenic transformation by MLL-fusion proteins in a fusion partner-independent manner , 2016, Leukemia.
[31] R. M. Owen,et al. An analysis of the attrition of drug candidates from four major pharmaceutical companies , 2015, Nature Reviews Drug Discovery.
[32] Bo Wen,et al. Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo. , 2015, Cancer cell.
[33] S. Armstrong,et al. AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes. , 2014, Cancer cell.
[34] E. Olhava,et al. DOT1L Inhibitor EPZ-5676 Displays Synergistic Antiproliferative Activity in Combination with Standard of Care Drugs and Hypomethylating Agents in MLL-Rearranged Leukemia Cells , 2014, The Journal of Pharmacology and Experimental Therapeutics.
[35] S. Bras,et al. Pontin is a critical regulator for AML1-ETO-induced leukemia , 2014, Leukemia.
[36] Phillip J. Wyss,et al. Discovery of MLL1 binding units, their localization to CpG Islands, and their potential function in mitotic chromatin , 2013, BMC Genomics.
[37] N. Perrimon,et al. FlyPrimerBank: An Online Database for Drosophila melanogaster Gene Expression Analysis and Knockdown Evaluation of RNAi Reagents , 2013, G3: Genes, Genomes, Genetics.
[38] E. Olhava,et al. Potent inhibition of DOT1L as treatment of MLL-fusion leukemia. , 2013, Blood.
[39] S. Armstrong,et al. Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l. , 2013, Blood.
[40] J. Rowley,et al. PBX3 is an important cofactor of HOXA9 in leukemogenesis. , 2013, Blood.
[41] S. Bray,et al. Notch cooperates with Lozenge/Runx to lock haemocytes into a differentiation programme , 2013, Development.
[42] H. Richardson,et al. An in vivo large-scale chemical screening platform using Drosophila for anti-cancer drug discovery , 2012, Disease Models & Mechanisms.
[43] A. Shilatifard,et al. The super elongation complex (SEC) family in transcriptional control , 2012, Nature Reviews Molecular Cell Biology.
[44] Jolanta Grembecka,et al. Menin-MLL inhibitors reverse oncogenic activity of MLL fusion proteins in leukemia. , 2012, Nature chemical biology.
[45] C. Allis,et al. Function of leukemogenic mixed lineage leukemia 1 (MLL) fusion proteins through distinct partner protein complexes , 2011, Proceedings of the National Academy of Sciences.
[46] Lars Bullinger,et al. MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L. , 2011, Cancer cell.
[47] S. Armstrong,et al. Selective killing of mixed lineage leukemia cells by a potent small-molecule DOT1L inhibitor. , 2011, Cancer cell.
[48] Yi Zhang,et al. DOT1L, the H3K79 methyltransferase, is required for MLL-AF9-mediated leukemogenesis. , 2011, Blood.
[49] U. Banerjee,et al. Genetic manipulation of AML1-ETO-induced expansion of hematopoietic precursors in a Drosophila model. , 2010, Blood.
[50] M. Diaz,et al. The PHD3 Domain of MLL Acts as a CYP33-Regulated Switch between MLL-Mediated Activation and Repression, , 2010, Biochemistry.
[51] V. Honti,et al. Cell lineage tracing reveals the plasticity of the hemocyte lineages and of the hematopoietic compartments in Drosophila melanogaster. , 2010, Molecular immunology.
[52] T. Dingermann,et al. The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4. , 2010, Blood.
[53] A. Shilatifard,et al. Linking H3K79 trimethylation to Wnt signaling through a novel Dot1-containing complex (DotCom). , 2010, Genes & development.
[54] A. Shilatifard,et al. AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia. , 2010, Molecular cell.
[55] O. Heidenreich,et al. A Drosophila model identifies calpains as modulators of the human leukemogenic fusion protein AML1-ETO , 2009, Proceedings of the National Academy of Sciences.
[56] Akihiko Yokoyama,et al. Menin critically links MLL proteins with LEDGF on cancer-associated target genes. , 2008, Cancer cell.
[57] A. Chinnaiyan,et al. A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification. , 2007, Blood.
[58] M. Cleary,et al. Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. , 2007, Genes & development.
[59] I. Andó,et al. Definition of Drosophila Hemocyte Subsets by Cell-Type Specific Antigens , 2007, Acta biologica Hungarica.
[60] V. Hartenstein,et al. A Hedgehog- and Antennapedia-dependent niche maintains Drosophila haematopoietic precursors , 2007, Nature.
[61] Matthew Meyerson,et al. The Menin Tumor Suppressor Protein Is an Essential Oncogenic Cofactor for MLL-Associated Leukemogenesis , 2005, Cell.
[62] Thomas A. Milne,et al. Physical Association and Coordinate Function of the H3 K4 Methyltransferase MLL1 and the H4 K16 Acetyltransferase MOF , 2005, Cell.
[63] C. J. Evans,et al. The Drosophila lymph gland as a developmental model of hematopoiesis , 2005, Development.
[64] Brian Stramer,et al. Live imaging of wound inflammation in Drosophila embryos reveals key roles for small GTPases during in vivo cell migration , 2005, The Journal of cell biology.
[65] V. Honti,et al. Characterization of the grappa Gene, the Drosophila Histone H3 Lysine 79 Methyltransferase , 2005, Genetics.
[66] R. Paro,et al. Expression of leukemic MLL fusion proteins in Drosophila affects cell cycle control and chromosome morphology , 2004, Oncogene.
[67] W. Herr,et al. Leukemia Proto-Oncoprotein MLL Forms a SET1-Like Histone Methyltransferase Complex with Menin To Regulate Hox Gene Expression , 2004, Molecular and Cellular Biology.
[68] Arndt Borkhardt,et al. Hoxa9 and Meis1 Are Key Targets for MLL-ENL-Mediated Cellular Immortalization , 2004, Molecular and Cellular Biology.
[69] A. Goto,et al. Drosophila hemolectin gene is expressed in embryonic and larval hemocytes and its knock down causes bleeding defects. , 2003, Developmental biology.
[70] R. Klapper,et al. The two origins of hemocytes in Drosophila , 2003, Development.
[71] N. Zeleznik-Le,et al. MLL repression domain interacts with histone deacetylases, the polycomb group proteins HPC2 and BMI-1, and the corepressor C-terminal-binding protein , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[72] C. Ferraz,et al. The Leucine Zipper Motif of the Drosophila AF10 Homologue Can Inhibit PRE-Mediated Repression: Implications for Leukemogenic Activity of Human MLL-AF10 Fusions , 2003, Molecular and Cellular Biology.
[73] Thomas A Milne,et al. MLL targets SET domain methyltransferase activity to Hox gene promoters. , 2002, Molecular cell.
[74] M. Birke,et al. The MT domain of the proto-oncoprotein MLL binds to CpG-containing DNA and discriminates against methylation. , 2002, Nucleic acids research.
[75] M. Diaz,et al. Protein Interactions of the MLL PHD Fingers Modulate MLL Target Gene Regulation in Human Cells , 2001, Molecular and Cellular Biology.
[76] R. Lanot,et al. Postembryonic hematopoiesis in Drosophila. , 2001, Developmental biology.
[77] C. Croce,et al. Upregulation of Meis1 and HoxA9 in acute lymphocytic leukemias with the t(4 : 11) abnormality , 2001, Oncogene.
[78] M. Cleary,et al. HoxA9-mediated immortalization of myeloid progenitors requires functional interactions with TALE cofactors Pbx and Meis , 2000, Oncogene.
[79] T Marty,et al. Regulation of Hox target genes by a DNA bound Homothorax/Hox/Extradenticle complex. , 1999, Development.
[80] J. Juang,et al. Dominant effects of the bcr-abl oncogene on Drosophila morphogenesis , 1999, Oncogene.
[81] J. Frestedt,et al. AF4 encodes a ubiquitous protein that in both native and MLL-AF4 fusion types localizes to subnuclear compartments. , 1998, Blood.
[82] S. Korsmeyer,et al. Altered Hox expression and segmental identity in Mll-mutant mice , 1995, Nature.
[83] D. Keene,et al. Peroxidasin: a novel enzyme‐matrix protein of Drosophila development. , 1994, The EMBO journal.
[84] H. Alder,et al. The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila trithorax, to the AF-4 gene , 1992, Cell.
[85] Michael L. Cleary,et al. Involvement of a homolog of Drosophila trithorax by 11q23 chromosomal translocations in acute leukemias , 1992, Cell.
[86] G. Evans,et al. A trithorax–like gene is interrupted by chromosome 11q23 translocations in acute leukaemias , 1992, Nature Genetics.
[87] R. Rizki,et al. Lamellocyte differentiation in Drosophila larvae parasitized by Leptopilina. , 1992, Developmental and comparative immunology.
[88] J. Rowley,et al. Identification of a gene, MLL, that spans the breakpoint in 11q23 translocations associated with human leukemias. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[89] L. Waltzer,et al. From Drosophila Blood Cells to Human Leukemia. , 2018, Advances in experimental medicine and biology.
[90] G. Sauvageau,et al. Human NUP98-HOXA9 promotes hyperplastic growth of hematopoietic tissues in Drosophila. , 2017, Developmental biology.
[91] V. Honti,et al. The cell-mediated immunity of Drosophila melanogaster: hemocyte lineages, immune compartments, microanatomy and regulation. , 2014, Developmental and comparative immunology.
[92] E. Lander,et al. MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia , 2002, Nature Genetics.
[93] I. Andó,et al. Supplemental Experimental Procedures Drosophila Strains , 2022 .